Enhanced lipid peroxidation in synoviocytes from patients with osteoarthritis

Brunella Grigolo, Livia Roseti, Mauro Fiorini, Andrea Facchini

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Objective. To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process. Methods. Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1β and tumor necrosis factor (TNF)-α stimulated cells. Results. Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions. Conclusion. In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.

Original languageEnglish
Pages (from-to)345-347
Number of pages3
JournalJournal of Rheumatology
Volume30
Issue number2
Publication statusPublished - Feb 1 2003

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Osteoarthritis
Lipid Peroxidation
Nitric Oxide
Rheumatoid Arthritis
Chondrocytes
Nitrites
Malondialdehyde
Interleukin-1
Synoviocytes
Nitrogen
Tumor Necrosis Factor-alpha

Keywords

  • Lipid peroxidation
  • Nitric oxide
  • Osteoarthritis
  • Rheumatoid arthritis
  • Synoviocytes

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

Cite this

Enhanced lipid peroxidation in synoviocytes from patients with osteoarthritis. / Grigolo, Brunella; Roseti, Livia; Fiorini, Mauro; Facchini, Andrea.

In: Journal of Rheumatology, Vol. 30, No. 2, 01.02.2003, p. 345-347.

Research output: Contribution to journalArticle

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abstract = "Objective. To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process. Methods. Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1β and tumor necrosis factor (TNF)-α stimulated cells. Results. Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions. Conclusion. In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.",
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N2 - Objective. To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process. Methods. Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1β and tumor necrosis factor (TNF)-α stimulated cells. Results. Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions. Conclusion. In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.

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